Traumatic brain injury represents the leading cause of death in young individuals. Various animal models have been developed to mimic human closed head injury (CHI). Widely used models induce head injury by lateral fluid percussion, a controlled cortical impact or impact acceleration. The presented model induces a CHI by a standardized weight-drop device inducing a focal blunt injury over an intact skull without pre-injury manipulations. The resulting impact triggers a profound neuroinflammatory response within the intrathecal compartment with high consistency and reproducibility, leading to neurological impairment and breakdown of the blood-brain barrier. In this protocol, we define standardized procedures for inducing CHI in mice and determine various severity grades of CHI through modulation of the weight falling height. In experienced hands, this CHI model can be carried out in as little as 30 s per animal, with additional time required for subsequent posttraumatic analysis and data collection.

In our experience, the prior practice of delayed cranioplasty (3-6 months postdecompressive craniectomy), requiring repeat hospital admission, does not seem to lower postcranioplasty infection rates nor the need for cerebrospinal fluid diversion procedures. Our current practice emphasizes cranioplasty during the initial hospital admission, as soon as there is resolution on computed tomography scan of brain swelling outside of the cranial vault with concurrent clinical examination. This occurs as early as 2 weeks postcraniectomy and should lower the overall cost of care by eliminating the need for additional hospital admissions.

Traumatic brain injury (TBI) represents a major health care problem and a significant socioeconomic challenge worldwide. In the United States alone, approximately 1.5 million patients are affected each year, and the mortality of severe TBI remains as high as 35%-40%. These statistics underline the urgent need for efficient treatment modalities to improve posttraumatic morbidity and mortality. Despite advances in basic and clinical research as well as improved neurological intensive care in recent years, no specific pharmacological therapy for TBI is available that would improve the outcome of these patients. Understanding of the cellular and molecular mechanisms underlying the pathophysiological events after TBI has resulted in the identification of new potential therapeutic targets. Nevertheless, the extrapolation from basic research data to clinical application in TBI patients has invariably failed, and results from prospective clinical trials are disappointing. We review the published prospective clinical trials on pharmacological treatment modalities for TBI patients and outline future promising therapeutic avenues in the field.

Background: Complement represents a crucial mediator of neuroinflammation and neurodegeneration after traumatic brain injury. The role of the terminal complement activation pathway, leading to generation of the membrane attack complex (MAC), has not been thoroughly investigated. CD59 is the major regulator of MAC formation and represents an essential protector from homologous cell injury after complement activation in the injured brain.

Therapeutic study, level III.

Therapeutic care/management, level III.

No abstract

We conclude the following: (a) anterior discectomy and fusion with a static (constrained) plating system is appropriate treatment for this type of injury, (b) in the absence of significant neurologic deficit with residual canal or foraminal stenosis, preoperative closed reduction is not necessary, (c) a small percentage of these patients will have vertebral artery injury, thus warranting screening with 16-slice computed tomographic angiography.